Calciseptine TFA
Based on 1 Customer Validation
Calciseptine TFA, a polypeptide found in black mamba venom, is a selcetive Cav1.2 L-type calcium channel inhibitor with an IC50 of 92 nM. Calciseptine TFA binds to the pore domain shoulder at repeats III and IV of Cav1.2, stabilizing an inactivated conformation. Calciseptine TFA exhibits negative inotropic and negative relaxant effects on mice, and does not affect heart rate or the action potential of sinoatrial node pacemaker cells. Calciseptine TFA can be used for the research of cardiovascular diseases.
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- Pureté : 97.55%
- Formule: C299H468N90O87S10.xC2HF3O2
- Masse moléculaire:7036.12 (free base)
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Stockage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
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Activité biologique
Description
IC50 & Target
[1]|
Cav1.2 92 nM (IC50) |
In Vitro
Calciseptine (100 nM-1 μM) TFA potently inhibits recombinant Cav1.2-mediated L-type Ca2+ currents in HEK-293T cells with an IC50 of 92 ± 18 nM, while having no significant effect on recombinant Cav1.342α- or Cav1.342-mediated currents at concentrations up to 1 μM[1].
Calciseptine (40-1000 nM) TFA inhibits Cav1.2 channel activity in HEK293T cells and 0.2 μM reducing peak Cav1.2 current by more than half[2].
Calciseptine TFA requires Cav1.2 residues Asp1117, Val1501, Asn1113, and Ala1123 for specific blockage of Cav1.2, as mutation of these residues reduces sensitivity Calciseptine[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Langendorff perfused hearts[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Isolated hearts from mice[1]
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Dosage:100 nM
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Administration:perfusion; continuous; 7 minutes
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Result:Reduced left ventricular contraction amplitude from 51±3 mmHg to 9±2 mmHg.
Decreased dP/dt max (contraction velocity) from 1.7±0.2 mmHg/ms to 0.4±0.1 mmHg/ms.
Decreased dP/dt min (relaxation velocity) from -1.2±0.1 mmHg/ms to -0.1±0.1 mmHg/ms.
Left baseline diastolic pressure unchanged (8±2 mmHg vs 8±3 mmHg).
Left averaged inter-beat (RR) intervals unaffected (273±17 ms vs 271±17 ms, p > 0.05).
Caused no arrhythmias during perfusion.
Chemical Information
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Appearance Solid
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Masse moléculaire 7036.12 (free base)
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Formule C299H468N90O87S10.xC2HF3O2
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Color White to off-white
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Sequence
Arg-Ile-Cys-Tyr-Ile-His-Lys-Ala-Ser-Leu-Pro-Arg-Ala-Thr-Lys-Thr-Cys-Val-Glu-Asn-Thr-Cys-Tyr-Lys-Met-Phe-Ile-Arg-Thr-Gln-Arg-Glu-Tyr-Ile-Ser-Glu-Arg-Gly-Cys-Gly-Cys-Pro-Thr-Ala-Met-Trp-Pro-Tyr-Gln-Thr-Glu-Cys-Cys-Lys-Gly-Asp-Arg-Cys-Asn-Lys (Disulfide bridge:Cys3-Cys22;Cys17-Cys39;Cys41-Cys52; Cys53-Cys58)
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Sequence Shortening
RICYIHKASLPRATKTCVENTCYKMFIRTQREYISERGCGCPTAMWPYQTECCKGDRCNK (Disulfide bridge:Cys3-Cys22;Cys17-Cys39;Cys41-Cys52; Cys53-Cys58)
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvant et solubilité
In Vitro:
H2O : ≥ 100 mg/mL
* "≥" means soluble, but saturation unknown.
Protocole
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Cardiac voltage-sensitive optical mapping
Cardiac voltage-sensitive optical mapping records changes in transmembrane potential from cardiac tissue by staining the preparation with a voltage-sensitive dye and imaging fluorescence changes during electrical activation; the resulting optical action potentials can be used to map activation time, action potential duration, conduction velocity, wavefront propagation, and arrhythmia dynamics. The optical signal represents a relative fluorescence change from a tissue volume rather than a single-cell intracellular recording, so spatial resolution, sampling rate, voltage resolution, optical magnification, light penetration, and motion control must be considered together when interpreting optical action potentials.
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Neuronal voltage-sensitive dye imaging
Neuronal voltage-sensitive dye imaging detects membrane-potential-dependent optical changes from dyes associated with neuronal membranes, enabling optical recording of electrical activity from single neurons, dendrites, axons, spines, or neuronal populations in brain slices and cultured neurons. VSD signals are typically reported as fractional fluorescence or absorbance changes over baseline, such as ΔF/F or ΔI/I, and published protocols use high-speed cameras or photodiode arrays because neuronal voltage signals occur on millisecond time scales. Fast VSD imaging can be applied at two common scales: bulk staining of brain slices to measure circuit-level spatiotemporal activity, and single-cell loading or biolistic delivery to record membrane-potential transients from individual neuronal compartments. Optical signals should be interpreted as membrane-potential-related readouts, and validation by simultaneous electrophysiology or pharmacological controls is recommended when the experimen
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Acute brain-slice whole-cell patch-clamp recording
Acute brain-slice whole-cell patch-clamp recording measures membrane voltage or ionic current from visually targeted cells in living brain slices; after giga-seal formation, the membrane under the pipette is ruptured to provide low-resistance electrical access to the cell interior, enabling current-clamp analysis of excitability and voltage-clamp analysis of synaptic or membrane currents. Acute slices preserve local tissue architecture better than dissociated preparations and allow visually guided recording from defined brain regions or fluorescently labeled cells; however, whole-cell access also permits exchange between pipette solution and cytoplasm, so intracellular dialysis must be considered when interpreting signaling-dependent phenomena.
Pureté et documentation
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Fiche technique (309 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Mesirca P, et al. Selective blockade of Cav1.2 (α1C) versus Cav1.3 (α1D) L-type calcium channels by the black mamba toxin calciseptine. Nat Commun. 2024 Jan 2;15(1):54. [Content Brief]
[2]. Gao S, et al. Structural basis for human Cav1.2 inhibition by multiple drugs and the neurotoxin calciseptine. Cell. 2023;186(24):5363-5374.e16. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)